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Related Concept Videos

Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
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Related Experiment Video

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Generation of Scaffold-free, Three-dimensional Insulin Expressing Pancreatoids from Mouse Pancreatic Progenitors In Vitro
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Rac1 regulates pancreatic islet morphogenesis.

Thomas U Greiner1, Gokul Kesavan, Anders Ståhlberg

  • 1Stem Cell and Pancreas Developmental Biology, Stem Cell Center, Lund University, BMC B10, Klinikgatan 26, SE-221 84 Lund, Sweden. thomas.greiner@med.lu.se

BMC Developmental Biology
|January 8, 2009
PubMed
Summary

Rac1 signaling is crucial for pancreatic islet cell migration during development. Blocking Rac1 inhibits beta cell movement and alters cell adhesion, impacting islet formation.

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05:38

Isolating and Analyzing Cells of the Pancreas Mesenchyme by Flow Cytometry

Published on: January 28, 2017

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Endocrinology

Background:

  • Pancreatic islets develop from ductal progenitors, involving cell delamination and migration.
  • Mechanisms controlling islet cell delamination and migration are not fully understood.
  • Rac1, a Rho GTPase, is known to regulate cell migration in various cell types.

Purpose of the Study:

  • To investigate the role of Rac1 in pancreatic islet morphogenesis and cell migration in vivo.
  • To elucidate the molecular mechanisms by which Rac1 influences islet cell behavior.

Main Methods:

  • Generated transgenic mice with dominant-negative Rac1 specifically in beta cells.
  • Assessed islet cell migration and spreading in vitro and in vivo.
  • Analyzed the effects of betacellulin on islet cells and measured E-cadherin expression.

Main Results:

  • Inhibition of Rac1 function in beta cells impaired their migration from the ductal epithelium.
  • Transgenic islet cells showed compromised spreading in vitro.
  • Betacellulin-induced actin remodeling and cell spreading were blocked in Rac1-deficient islets.
  • Blocking Rac1 activity led to increased E-cadherin-mediated cell-cell adhesion.

Conclusions:

  • Rac1 signaling is essential for regulating islet cell migration via E-cadherin-mediated adhesion.
  • Betacellulin may act as an in vivo regulator of Rac1 activity and islet cell migration.
  • Rac1 is a key regulator of cell migration and adhesion in tissue morphogenesis.